Related Experiment Video
Updated: Feb 5, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Regulation of apoptosis-related genes during interactions between oyster hemocytes and the alveolate parasite
Yuk-Ting Lau1, Bianca Santos1, Michelle Barbosa1
1School of Marine and Atmospheric Sciences, Stony Brook University, Stony Brook, NY, 11794, United States.
Abstract:
The alveolate Perkinsus marinus is the most devastating parasite of the eastern oyster Crassostrea virginica. The parasite is readily phagocytosed by oyster hemocytes, but instead of intracellular killing and digestion, P. marinus can survive phagocytosis and divide in host cells. This intracellular parasitism is accompanied by a regulation of host cell apoptosis. This study was designed to gain a better understanding of the molecular mechanisms of apoptosis regulation in oyster hemocytes following exposure to P. marinus. Regulation of apoptosis-related genes in C. virginica, and apoptosis-regulatory genes in P. marinus, were investigated via qPCR to assess the possible pathways involved during these interactions. In vitro experiments were also carried out to evaluate the effect of chemical inhibitors of P. marinus antioxidant processes on hemocyte apoptosis. Results indicate the involvement of the mitochondrial pathway (Bcl-2, anamorsin) of apoptosis in C. virginica exposed to P. marinus. In parallel, the antioxidants peroxiredoxin and superoxide dismutase were regulated in P. marinus exposed to C. virginica hemocytes suggesting that apoptosis regulation in infected oysters may be mediated by anti-oxidative processes. Chemical inhibition of P. marinus superoxide dismutase resulted in a marked increase of reactive oxygen species production and apoptosis in infected hemocytes. The implication of oxygen-dependent apoptosis during P. marinus infection and disease development in C. virginica is discussed.
Insights
Perkinsus marinus evades oyster immune cells by regulating apoptosis. Inhibiting parasite antioxidants increases reactive oxygen species and oyster cell death, suggesting a novel therapeutic target for oyster disease.
Area of Science:
- Marine biology and immunology
- Parasitology and host-pathogen interactions
- Molecular mechanisms of apoptosis
Background:
- Perkinsus marinus is a major pathogen of the eastern oyster, Crassostrea virginica.
- P. marinus survives phagocytosis by oyster hemocytes, leading to intracellular parasitism.
- This intracellular survival is linked to the regulation of host cell apoptosis.
Purpose of the Study:
- To elucidate the molecular mechanisms of apoptosis regulation in oyster hemocytes during P. marinus infection.
- To investigate the roles of oyster apoptosis-related genes and parasite apoptosis-regulatory genes.
- To evaluate the impact of inhibiting P. marinus antioxidant processes on hemocyte apoptosis.
Main Methods:
- Quantitative PCR (qPCR) to assess gene expression in Crassostrea virginica and P. marinus.
- In vitro experiments using chemical inhibitors targeting P. marinus antioxidant pathways.
- Measurement of reactive oxygen species (ROS) production and hemocyte apoptosis.
Main Results:
- Evidence for the involvement of the mitochondrial apoptosis pathway (Bcl-2, anamorsin) in C. virginica hemocytes.
- Regulation of antioxidant genes (peroxiredoxin, superoxide dismutase) in P. marinus upon interaction with hemocytes.
- Chemical inhibition of P. marinus superoxide dismutase significantly increased ROS and hemocyte apoptosis.
Conclusions:
- Apoptosis regulation during P. marinus infection may involve parasite anti-oxidative processes.
- Oxygen-dependent apoptosis is implicated in P. marinus infection and disease progression in oysters.
- Targeting parasite antioxidant mechanisms presents a potential strategy for managing oyster disease.
Related Concept Videos
Gene Regulation During Sporulation
Negative Regulator Molecules
Circadian Rhythms and Gene Regulation
Constitutive and Regulated Gene Expression
Gene-Environment Interactions
Apoptosis

